Functional capabilities of the papillary muscles of the left heart in rats during adaptation to high altitude conditions]

This study describes seven patients with the mitral valve prolapse or click-murmur syndrome who have survived one or more episodes of life-threatening ventricular arrhythmias. These arrhythmias include cardiac arrest due to ventricular fibrillation, recurrent ventricular tachycardia causing syncope or sustained ventricular tachycardia requiring electroversion. These patients were seen over a two-year period in a single medical center. Five of the seven had repolarization abnormalities in the resting electrocardiogram. Premature ventricular contractions were present in the routine resting electrocardiograms of six of the seven patients and were frequent during treadmill testing and ambulatory electrocardiographic monitoring in all six tested. There were electrolyte abnormalities or changes in medications known to affect myocardial repolarization during the week before the episode in three of the four patients with cardiac arrest. The diagnosis of mitral valve prolapse click-murmur syndrome was made prior to the episode of life-threatening arrhythmia in only two of the seven patients. Varying forms of antiarrhythmic therapy were given to these patients during follow-up periods of five to 26 months. Although the incidence of fatal arrhythmias in the mitral prolapse syndrome is probably small, we suggest that such arrhythmias may not be extremely rare, particularly among those patients who have repolarization abnormalities in the resting electrocardiogram and frequent premature beats. Patients with unexplained ventricular arrhythmias should be screened for mitral valve prolapse.     

Aneurysm of the splenic artery

Electrocardiographic abnormalities had been reported, in patients with subarachnoid hemorrhage, with variable percentage from 2% to 91%, according to several studies. The most common changes are T wave inversion, ST segment elevation or depression, QT prolongation, U waves, atrial flutter and fibrillation, ventricular fibrillation, supraventricular tachycardia, premature atrial and ventricular contractions. These findings occur within the first forty-eight hours after the onset of the symptoms; they usually are benign and transient. In a small percentage of cases generally in severe ESA, the ECG changes are associated with ventricular asynergy, coronary vasospasm or subendocardic necrosis. The arrhythmias could be produced either by autonomic discharges to the heart, during increased sympathetic activity due to ESA, or by a damage of cerebral areas with arrhythmogenic capacity. The importance of ECG abnormalities towards mortality and morbidity in patients with ESA has not yet been cleared; however, a careful monitoring is recommended to prevent severe cardiac complications and to obtain an indirect, further evaluation of the neurologic pathology.     

Ventricular arrhythmias in syndrome of balloon deformity of mitral valve. Definition of possible high risk group

Twenty patients clinically identified as having balloon deformity of the mitral valve were studied to assess the incidence of ventricular arrhythmias. Echocardiography and phonocardiography were used to confirm the nature of the mitral valve lesion. Continuous 24-hour electrocardiograms were obtained from all patients and analysed by a computer and 2 observers. One patient has ventricular fibrillation and 3 patients had ventricular tachycardia. There was a high incidence of other less severe forms of ventricular arrhythmias. Eight patients had inferolateral ST and T wave abnormality on the resting electrocardiogram, and were described as having the ausculatatory-electrocardiographic variant of the balloon mitral valve syndrome. The occurrence of serious ventricular arrhythmias (ventricular fibrillation and tachycardia) was significantly more frequent in this group. This raises the possibility that the resting electrocardiogram may identify those patients with balloon deformity of the mitral valve who are at risk from sudden death.     

Use of bovine heterografts in intravenous therapy

Severe prolapse of the mitral valve leaflets was seen at left ventricular angiography in 16 of 92 patients with a secundum type atrial septal defect studied prospectively from 1970 to 1974. The patients were aged 15 to 69 years; angioplasty or mitral valve replacement was carried out in nine. In 9 of 122 patients aged 15 to 55 years who were operated on for closure of a secundum type atrial septal defect between 1956 and 1969, mitral regurgitation due to prolapse but with intact chordae tendineae was seen at operation. In three of these patients chordal rupture was seen at a second operation 2 to 6 years later. The outlook in the syndrome of mitral valve prolapse may be less benign than is usually believed.     

Anesthesia case of the month. Analgesia for fractures until surgery can take place

OBJECTIVE: To emphasize a potentially lethal condition that is virtually impossible to diagnose preoperatively. DESIGN: Case report with review of the literature. SETTING: University Hospital. PARTICIPANT: The patient requiring urgent surgery for heart failure related to severe aortic stenosis and mild mitral stenosis with poor ventricular function. The patient was elderly and suffered from atrial fibrillation. INTERVENTIONS: Preoperative transesophageal echocardiography followed by mitral valve repair and aortic valve replacement. MEASUREMENTS: Clinical outcome and pathological results. RESULTS: Although preoperative TEE demonstrated no left atrial appendage abnormality. After cardiac manipulation prior to the institution of cardiopulmonary bypass a large left atrial mural thrombus was mobilized from the atrial wall and was free floating in the left atrium. CONCLUSIONS: For high risk patients TEE should be applied intraoperatively to avoid undiagnosed left atrial clot dislodgement.     

Is atrial fibrillation resulting from rheumatic mitral valve disease a proper indication for the maze procedure?

BACKGROUND: There are a few patients without detectable atrial contraction despite restoration of atrial rhythm after the maze procedure for atrial fibrillation (AF) associated with mitral valve disease. METHODS: From January 1995 to March 1997, 29 consecutive patients with AF associated with mitral valve disease underwent our modified maze procedure combined with mitral or other valve operations. The causes of mitral valve disease were rheumatic mitral stenosis (n = 22) and nonrheumatic mitral regurgitation (n = 7). The 17 patients with postoperative atrial rhythm were divided into group I with rheumatic mitral stenosis (n = 10), and group II with mitral regurgitation of nonrheumatic origins (n = 7). RESULTS: Seventeen patients regained atrial rhythm, 2 patients had junctional rhythm, and another 10 remained in AF. Between the group of patients with restoration of atrial rhythm and that of patients remaining in AF, significant differences were found in the percentage with rheumatic disease, history of AF, and maximum f-wave voltage. The postoperative peak velocity of the atrial filling wave to peak velocity of early filling wave ratio for the left atrium measured using Doppler echocardiography was 0.25 in group I, which was significantly lower than that (0.42) in group II. CONCLUSIONS: Reconsideration of the indications for the maze procedure for AF associated with rheumatic mitral stenosis may thus be reasonable, particularly for cases in which replacement using a prosthetic valve is necessary, but we believe that patients with nonrheumatic mitral valve disease, especially those able to undergo reconstructive operations, are the best candidates for the maze procedure.     

Interference of mitral valve stenosis with left ventricular diastole and left atrial appendage flow

Atrial fibrillation (AF) has been reported as an independent risk factor of systemic thromboembolism. Almost half of the left atrial thrombi are located in the left atrial appendage (LAA). LAA function, reflected by LAA flow, thus has an influence on the potential of distal embolic complications. To identify factors other than atrial contraction that influence LAA flow during AF, transthoracic and transesophageal echocardiographic studies were performed on 130 patients. Seventy patients with nonrheumatic AF were divided into two groups with higher peak LAA outflow velocity (group 1) and lower peak LAA outflow velocity (group 2) at the ventricular systolic phase. Sixty patients with rheumatic AF were classified as group 3. Group 1 had a higher peak LAA outflow velocity than group 2 at both the ventricular systolic and diastolic phases. Group 2 had a higher peak LAA outflow at the ventricular diastolic phase than group 3 (18.9 +/- 8.0 vs. 11.8 +/- 7.5 cm/s, p < 0.001), whereas there was no significant difference in the peak LAA outflow at the ventricular systolic phase between the two groups (9.6 +/- 4.0 vs. 10.8 +/- 6.8 cm/s, p = NS). Group 3 was subdivided according to mitral valve area. Patients with severe mitral stenosis (mitral valve area < 1 cm2) had a significantly lower diastolic augmentation of LAA outflow velocity (difference of LAA outflow velocity between ventricle systole and diastole) than patients with mild to moderate stenosis (0.5 +/- 3.2 vs. 2.6 +/- 4.9 cm/s, p < 0.05). In conclusion, patients with rheumatic AF, especially those with severe mitral stenosis, have a lower diastolic augmentation of LAA outflow velocity. The lower diastolic augmentation of the LAA outflow velocity at the ventricular diastolic phase might result from interference with the suction effect of the left ventricular diastole by the stenotic mitral valve.     

Estimation of left ventricular end-diastolic pressure with the difference in pulmonary venous and mitral A durations is limited when mitral E and A waves are overlapped

Previous studies showed that difference in pulmonary venous and mitral A-wave durations can be used for the estimation of left ventricular end-diastolic pressure, which is based on the assumption that the pulmonary venous A wave and mitral A wave start with the beginning of left atrial contraction. It is also assumed that the mitral A wave ends with the end of left atrial contraction. These assumptions may not be correct if left atrial contraction occurs before the early left ventricular filling is completed. Adequate Doppler mitral inflow and pulmonary venous flow signals were obtained simultaneously with left ventricular pressures at the cardiac catheterization laboratory in 50 patients who showed separated E and A waves in mitral inflow. After heart rate was increased by right atrial pacing to make the mitral E and A waves overlap, Doppler and hemodynamic measurements were repeated. When E and A waves are separated, pulmonary A-wave duration exceeding mitral A-wave duration has a sensitivity of 67% and specificity of 85% in the prediction of elevated left ventricular end-diastolic pressure (>/=20 mm Hg), whereas the pulmonary A wave ending later than mitral A wave has a sensitivity of 83% and a specificity of 45%. When the mitral E and A waves are overlapped, the pulmonary A wave ending later than mitral A wave is better for the prediction of elevated left ventricular end-diastolic pressure (sensitivity 55%, specificity 75%) than pulmonary A-wave duration exceeding mitral A-wave duration (sensitivity 9%, specificity 96%). However, overall, both methods are limited for clinical use.     

Noonan syndrome: structural abnormalities of the mitral valve causing subaortic obstruction

Among 41 consecutive children with classic Noonan syndrome, 27 patients (66%) presented cardiac anomalies. Eight patients (19.5%) had a congenital anomaly of the mitral valve consisting of 5 with partial atrioventricular canal defect and 3 with anomalous insertion of the mitral valve on the ventricular septum. Five patients (12%) presented with a significant left ventricular outflow tract obstruction caused by the anterior leaflet of the mitral valve: two cases with atrioventricular canal and three cases with isolated anomalous insertion of the mitral valve. Echocardiography is the best tool for the diagnosis. Cardiac defects of patients with Noonan syndrome may be explained on the basis of anomalies of the extracellular matrix involving cardiac valves including the mitral valve. CONCLUSION: In children with Noonan syndrome and left ventricular hypertrophy a careful echocardiographic assessment of the mitral valve should reveal those in whom the left ventricular outflow tract obstruction is anatomical in nature.     

Ventricular buckling: a factor in the abnormal ventriculogram and peculiar hemodynamics associated with mitral valve prolapse

Because of intractable ventricualr arrhythmias after a near-fatal episode of ventricular fibrillation, a patient with idiopathic mitral valve prolapse was subjected to mitral valve replacement. Vector analysis and intraoperative epicardial mapping localized the ectopic focus to the region of the posterior papillary muscle. The patient is alive and well two years after surgery; chronically inverted T waves have become upright. But propranolol and diphenylhydantoin are needed to prevent arrhythmias and T wave abnormalities during standing and exercise. Preoperatively, with the onset of mitral regurgitation and a second rapid phase of prolapse, the ventriculogram was deformed by abnormal midsystolic hyperkinesis at both sites of papillary muscle insertion. Postoperatively, focal hypokinesis appeared in the same areas, implying that they had been retracted by the prolapsing valve. Preoperatively, a papillary tip could be seen entering the mitral ring while coronary arteriography showed late systolic elongation of a small vessel feeding the anterior papillary muscle, suggesting that the papillary apparatus was indeed subject to damaging stress during the abnormal basal movement. Three other persons with severe mitral prolapse (but intact chordae) have had valve repacement and developed qualitatively similar changes in the ventriculogram. Papillary speciments in two showed significant fibrosis. Indication for operation in one of these was edpisodic ventricular fibrillation, which has not recurred. A spectrum of ventriculographic abnormality associated with mitral prolapse could be partly explained by hypokinesis of the papillary loops, variably disguised by retraction stress tansmitted from the billowing leaflets, translocation of blood into the expanding valve sail, and various degrees of unloading into the left atrium. Abnormal intraventicular flow may probably result from associated prolapse of the anterior leaflet and from buckling of the papillary sties toward the mitral annulus. Unusual physical findings in the operated cases and in eight other patients define a clinically recognizable syndrome in which severe prolapse abbreviates left ventricular ejection. Liability to symptoms and to progression of disease seems high in this group.     

Apical cross-sectional echocardiography. Standard for the diagnosis of idiopathic mitral valve prolapse syndrome

In light of the nonspecificity of left ventricular angiography and physical examination, and the limitations of M-mode echocardiography to define the presence of mitral valve prolapse syndrome, we evaluated left ventricular longitudinal and apical four-chamber tomographic views of cross sectional echocardiography in 19 subjects with normal left ventricular cineangiography and in 5 patients with congestive cardiomyopathy. None had auscultatory findings suggestive of mitral valve prolapse syndrome. In all 24 control subjects, the apical view demonstrated the coaptation point and the leaflets of the mitral valve to lie inside the left ventricular cavity. A retrospective analysis of 900 consecutive cross sectional echocardiographic studies revealed 105 subjects with no evidence of structural heart disease other than the presence of the mitral valve leaflets in the left atrium in systole defining the existence of idiopathic mitral valve prolapse syndrome. Both mitral leaflets were prolapsed in 90 percent of the involved populations, and the apical tomographic cross sectional echocardiographic view was superior to the left ventricular longitudinal view for the detection of anterior leaflet prolapse. These data suggest that the apical cross sectional view may be the single best technique to define the presence of idiopathic mitral valve prolapse syndrome.     

Flutter of left ventricular structures in patients with aortic regurgitation, with special reference to patients with associated mitral stenosis

Echocardiography was performed in 45 patients with aortic regurgitation. Forty showed a high frequency diastolic flutter of the mitral valve, which was holodiastolic in all but the patients with associated mitral stenosis. Of four patients with coexisting mitral stenosis, mitral flutter was absent in two; in the other two, in atrial fibrillation, mitral flutter occurred, but only during a fixed interval after mitral valve opening, irrespective of cycle length. A fine flutter of similar frequency was observed on the left ventricular aspect of the ventricular septum in 12 patients. In six of these it was of slight degree and restricted to early diastole and the high septum; in four others (three of whom had associated mitral stenosis), the septal flutter was more marked, holodiastolic, and present over all parts of the septum scanned; in two, it was holodiastolic over the high septum but early diastolic at lower septal levels. Aortography performed in 19 patients showed that septal flutter was present in seven of 12 patients in whom the regurgitant aortic jet was directed forward to the ventricular septum, whereas in the other seven patients with no septal flutter, the jet was directed away from the septum. Septal flutter is useful as an echocardiographic sign of aortic regurgitation, especially in the presence of mitral stenosis when mitral flutter may be absent or exceeded by septal flutter in both amplitude and duration, and when the mitral valve has been replaced by a prosthetic valve. Vibration of the septum appears to be attributable to the regurgitant aortic jet impinging on it and may contribute to the production and radiation of the characteristic diastolic murmur of aortic regurgitation.     

Non-obstructive hypertrophic cardiomyopathy with mitral regurgitation requiring valve replacement

Non-obstructive hypertrophic cardiomyopathy (HCM) is rarely associated with mitral regurgitation severe enough to require valve replacement. A 39-year-old man, previously diagnosed as having non-obstructive HCM with mitral regurgitation, developed atrial fibrillation with tachycardia and congestive heart failure. Echocardiography and cardiac catheterization, including left ventriculography, documented an unusual type of non-obstructive HCM with severe mitral regurgitation. The patient underwent successful mitral valve replacement.     

The first original Russian class-III antiarrhythmic nibentan

The paper presents experimental and clinical findings of the new antiarrhythmic drug nibentan. The agent was found to be a class-III antiarrhythmic agent in terms of its electrophysiological effects and an inhibitor of the delayed rectifier potassium current in terms of its effects on the ionic channels of cardiomyocytes. The clinical trial of nibentan shows that the drug is highly effective (in 70-100% of cases) in patients with atrial flutter and fibrillation and in those with supraventricular tachycardia and it is less effective in suppressing ventricular premature contractions and tachycardia. The rate of arrhythmogenic effects produced by the drug was inversely related to its antiarrhythmic action. Nibentan has been approved for clinical use.     

Atrial fibrillation in Wolff-Parkinson-White syndrome. Development and therapy

In patients with Wolff-Parkinson-White syndrome the accessory pathway may participate in various tachyarrhythmias thereby influencing symptoms and prognosis. Atrial fibrillation occurs in 10 to 32% of patients and may have life-threatening consequences by precipitating ventricular fibrillation in patients with rapid conduction due to an accessory pathway with short anterograde refractory period (< 250 ms). Pathogenesis of atrial fibrillation in the WPW syndrome and therapeutic options are reviewed in this presentation. Spontaneous degeneration of atrioventricular reentrant tachycardia has been reported to represent the most frequent mode of initiation of atrial fibrillation during electrophysiologic study (up to 64% of episodes). Hemodynamic changes during tachycardia may lead to increased sympathetic tone, hypoxemia or increased tension of the atrial wall, thus, triggering atrial fibrillation. Induction of reentrant tachycardia during electrophysiologic study also has shown to be strongly correlated to its clinical prevalence and is inducible in up to 77% of patients with atrial fibrillation. The pathogenesis and high incidence of atrial fibrillation in patients with WPW syndrome is related to presence and functional properties of the accessory pathway. After surgical excision or catheter ablation more than 90% of patients are free of this arrhythmia. Anterograde conduction properties of the pathway appear to be more important than retrograde properties. High incidence of atrial fibrillation is related to short anterograde refractory periods, and of note, this arrhythmia is rare (3%) in patients with concealed pathways. With intracardiac recordings, Jackman et al. could demonstrate atrial fibrillation due to micro-reentry originating in accessory pathway networks.(ABSTRACT TRUNCATED AT 250 WORDS)     

Congenital complete atrioventricular block and prolapsing mitral valve

Congenital complete atrioventricular block and prolapsing mitral valve are described in a 41-year-old woman who exhibited ventricular arrhythmias and symptoms initially attributed to her atrioventricular block. The importance of physical examination to elicit clues in the diagnosis of prolapsing mitral valve is emphasized.     

Left atrial spontaneous contrast echoes--markers of thromboembolic risk in patients with atrial fibrillation

A consecutive series of 80 patients with atrial fibrillation were studied with both precordial and transoesophageal echocardiography. Left atrial spontaneous contrast echoes were observed in one patient with precordial echocardiography and in 26 patients (33%) with transoesophageal echocardiography. They were found most commonly in patients with rheumatic mitral valve disease (67%) but were observed in 28% of patients with lone atrial fibrillation. Their presence was unrelated to the age, gender and therapy of the patient. Although they were more common in patients with a large left atrium, they were sometimes observed in a normal sized atrial chamber. They were more common in chronic (40%) than in paroxysmal atrial fibrillation (5.6%). No patient had severe mitral regurgitation, but contrast echoes were observed in some patients with mild or moderate mitral regurgitation. Of the 26 patients with spontaneous contrast echoes, six (23%) had echoes consistent with left atrial thrombus compared to one of the 54 patients without these echoes (1.9%) (P = 0.006); 17 (65%) had suffered a previous thromboembolic event compared to 17 of the 54 without these echoes (32%) (P = 0.009). These data support the concept that spontaneous contrast echoes in the left atrium are associated with sluggish blood flow and a thrombogenic environment. Transoesophageal echocardiography may thus be useful in assessing which patients with atrial fibrillation might most benefit from anticoagulation. This hypothesis needs to be evaluated further in a prospective study.     

Exhaustion of vascular endowment in hemodialysis: proposal for a permanent inlet access

A simple left atrial procedure for atrial fibrillation (AF) was performed in 16 elderly patients (age over 70 years old) with chronic AF associated with mitral and/or aortic valvular diseases. Chronic AF was eliminated upon discharge in 13 out of the 16 patients (81%). Twelve of the 13 patients (92%) whose AF had disappeared recovered the atrial kick of their right atrium, and 9 patients (70%) recovered the atrial kick of their left atrium. A simple surgical procedure to the left atrium was effective in the treatment of chronic AF associated with mitral valve disease in elderly patients. This simple procedure is preferable to other methods for the elimination of chronic AF with mitral valve disease in elderly patients.     

DNA ploidy and expression of p53 and C-erbB-2 in extramammary Paget''s disease of the vulva

We report a case of total pulse alternans in a patient with paroxysmal ectopic atrial tachycardia and echocardiographic findings obtained before and after radiofrequency catheter ablation (RFCA) that terminated the arrhythmia. The patient was a 27-year-old man with history of paroxysmal palpitations with worsening episodic dizziness, chest tightness, and dyspnea. Electrocardiography (ECG) showed atrial tachycardia at 160 to 170 beats/min while the simultaneous pulse was in the 80s beats/min. Echocardiogram showed that aortic and mitral valves opened with alternating excursions and outflow velocities. Furthermore, despite similar ventricular wall thickening during systole of consecutive cardiac cycles, there was alternating mitral valve opening during diastole of the same cycles, providing direct evidence that ineffective diastolic filling and mitral valve opening may play a role in the pathogenesis of pulse alternans. Repeat ECG and echocardiography after the successful RFCA showed normal sinus rhythm and normal opening excursion and the velocity across the aortic and mitral valves.     

Estimation of left ventricular filling pressures using two-dimensional and Doppler echocardiography in adult patients with cardiac disease. Additional value of analyzing left atrial size, left atrial ejection fraction and the difference in duration of pulmonary venous and mitral flow velocity at atrial contraction

OBJECTIVES: The purpose of this study was to determine whether left atrial size and ejection fraction are related to left ventricular filling pressures in patients with coronary artery disease. BACKGROUND: In patients with coronary artery disease, left ventricular filling pressures can be estimated by using Doppler mitral and pulmonary venous flow velocity variables. However, because these flow velocities are age dependent, additional variables that indicate elevated left ventricular filling pressures are needed to increase diagnostic accuracy. METHODS: Echocardiographic left atrial and Doppler mitral and pulmonary venous flow velocity variables were correlated with left ventricular filling pressures in 70 patients undergoing cardiac catheterization. RESULTS: Left atrial size and volumes were larger and left atrial ejection fractions were lower in patients with elevated left ventricular filling pressures. Mean pulmonary wedge pressure was related to mitral E/A wave velocity ratio (r = 0.72), left atrial minimal volume (r = 0.70), left atrial ejection fraction (r = -0.66) and atrial filling fraction (r = -0.66). Left ventricular end-diastolic and A wave pressures were related to the difference in pulmonary venous and mitral A wave duration (both r = 0.77). By stepwise multilinear regression analysis, the ratio of mitral E to A wave velocity was the most important determinant of pulmonary wedge (r = 0.63) and left ventricular pre-A wave (r = 0.75) pressures, whereas the difference in pulmonary venous and mitral A wave duration was the most important variable for both left ventricular A wave (r = 0.75) and left ventricular end-diastolic (r = 0.80) pressures. The sensitivity of a left atrial minimal volume > 40 cm3 for identifying a mean pulmonary wedge pressure > 12 mm Hg was 82%, with a specificity of 98%. CONCLUSIONS: Left atrial size, left atrial ejection fraction and the difference between mitral and pulmonary venous flow duration at atrial contraction are independent determinants of left ventricular filling pressures in patients with coronary artery disease. The additive value of left atrial size and Doppler variables in estimating filling pressures and the possibility that left atrial size may be less age dependent than other mitral and pulmonary venous flow velocity variables merit further investigation.